Researchers at Ohio State University have revealed that an early and strong immune response might help curb the infection, that is likely to last long, against retroviruses such as HIV and HTLV-1 that don't hit-and-run, they hit-and-hide.
According to the researchers, cancer viruses slip into host cells and insert their own DNA into the cell's DNA, and from this refuge they establish an infection that lasts a lifetime.
"Our findings indicate that if the immune system could respond strongly to HTLV-1 and kill infected target cells early, it may inhibit the virus's ability to establish reservoirs of infected cells and make the infection more manageable later," said principal investigator Michael Lairmore, a professor and chair of veterinary biosciences and a cancer researcher at OSUCCC-James.
"This study tells us that the more we know about the earliest events of infection, the more it will help us develop vaccines and might block those events," Lairemore added.
Lairmore and his colleagues examined HTLV-I infection in rabbits that were treated with the drug cyclosporin A, which is commonly used to suppress the immune system in people following organ transplantation.
They compared animals treated with this drug prior to viral infection with those given the drug one week after infection.
In animals given the immune-suppressing drug first, the virus flourished. The number of virus copies jumped to 200 per 10,000 immune cells (lymphocytes), compared with 40 per 10,000 immune cells in control animals (these were infected with the virus but not given the drug).
After a week or two, the number of virus copies fell, ranging from 113 to 160 for remainder of the 10-week experiment.
In the animals that were given the virus first and then the immune-suppressing drug a week later, on the other hand, the virus languished.
"The first experiment told us that if the immune system is suppressed, the viral load goes up - and we expected that," said Lairmore.
"The second group was the surprise. Their viral load was low from the start, and it stayed that way. We didn't expect that. We thought the virus would recover and come back up.
"Collectively, our findings indicate that the immune system plays a key role in controlling HTLV-1 spread during early infection, which has important implications for a vaccine against this virus and for therapy for HTLV-1-associated diseases," he added.